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10.1016/j.ijid.2020.05.110

http://scihub22266oqcxt.onion/10.1016/j.ijid.2020.05.110
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32497811!7264936!32497811
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suck abstract from ncbi


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pmid32497811      Int+J+Infect+Dis 2020 ; 97 (ä): 303-305
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  • Iron: Innocent bystander or vicious culprit in COVID-19 pathogenesis? #MMPMID32497811
  • Edeas M; Saleh J; Peyssonnaux C
  • Int J Infect Dis 2020[Aug]; 97 (ä): 303-305 PMID32497811show ga
  • The coronavirus 2 (SARS-CoV-2) pandemic is viciously spreading through the continents with rapidly increasing mortality rates. Current management of COVID-19 is based on the premise that respiratory failure is the leading cause of mortality. However, mounting evidence links accelerated pathogenesis in gravely ill COVID-19 patients to a hyper-inflammatory state involving a cytokine storm. Several components of the heightened inflammatory state were addressed as therapeutic targets. Another key component of the heightened inflammatory state is hyper-ferritinemia which reportedly identifies patients with increased mortality risk. In spite of its strong association with mortality, it is not yet clear if hyper-ferritinemia in COVID-19 patients is merely a systemic marker of disease progression, or a key modulator in disease pathogenesis. Here we address implications of a possible role for hyper-ferritinemia, and altered iron homeostasis in COVID-19 pathogenesis, and potential therapeutic targets in this regard.
  • |Betacoronavirus[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/mortality/*pathology[MESH]
  • |Cytokine Release Syndrome/virology[MESH]
  • |Ferroptosis[MESH]
  • |Hepcidins/physiology[MESH]
  • |Humans[MESH]
  • |Inflammation[MESH]
  • |Iron Overload/*virology[MESH]
  • |Iron/blood[MESH]
  • |Mitochondria/pathology/physiology[MESH]
  • |Oxidative Stress[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/mortality/*pathology[MESH]


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